Tuesday, November 21, 2017

In the News: DNAJB9- a novel autoantigen staining for Fibrillary GN

A new paradigm shift in diagnosis of Fibrillary GN(FGN) has occurred. This rare form of organized deposit related GN might have a pathology staining marker in the making.
Through the use of laser microdissection assisted liquid chromatography tandem mass spectrometry , The Mayo pathologist  recently discovered a novel proteomic biomarker for FGN: DnaJ homolog subfamily B member 9 (DNAJB9), a member of the molecular chaperone gene family. When looking at specific biopsy samples of FGN vs non FGN cases, strong, homogeneous, smudgy DNAJB9 staining of glomerular deposits was seen in all but 2 cases of FGN in one report published in KI-R.

This test had a 98% sensitivity and > 99% specificity. Immunoelectron microscopy showed localization of DNAJB9 to FGN fibrils but not to amyloid fibrils or immunotactoid glomerulopathy microtubules. (http://www.kireports.org/article/S2468-0249(17)30341-8/pdf)

Another similar manuscript in JASN showed the same finding. 






Looks like we may have a diagnostic test and catch more cases of FGN 

Saturday, November 18, 2017

TOPIC DISCUSSION: Diuresis in CHF

An amazing article this month in NEJM discusses Diuretic use in CHF- a must read for Cardiologist and Nephrologists.

Some interesting take home points:

1. Diuretic resistance causes: Non adherence, gut edema, impaired diuretic secretion due to CKD or aging, hypoproteinemia, hypotension, nephrotic syndrome, use of NSAIDS, low renal blood flow, nephron remodeling and neurohormonal activation.

2. Bumetanide and torsemide have higher and more consistent oral bioavailability over furosemide and make oral and IV doses kinetics similar( often under utilized by many)

3. Torsemide has the longest half life of all loop diuretics-- 6 hours.

4. Two forms of adaptations: a) A dose of loop diuretic increases urinary Na loss for few hours but then is followed by a period of very low sodium excretion often called " post diuretic Na retention". When dietary Na intake is high, the post diuretic Na retention effect will offset the initial natriuresis. 
The second is braking phenomenon.  When diuresis happens and fluid volume declines, this activates the SNS and RAS leading to nephron remodeling( distal nephron hypertrophy). This is a helpful thing to put brakes on the severe contraction of the ECF. But when this occurs in a patient that is volume overloaded, it's causing harm.

5. Treatment should aim for daily urine volume of 3-5L till euvolemia.  A stepped wise approach is suggested in bolus of furosemide followed by drip if needed. Metolazone or HCTZ( high dose) can be used as additional agents.

6. Tolvaptan: Data is mixed and can be used in some especially if Na issues are also a concern
7. Dopamine and Nesirtide - no data to support use
8. Aldactone didn't improve outcomes in acute CHF patients that require aggressive diuresis
9. Diuretic Resistance: Failure of diuretics to achieve decongestion, so with max doses you still get a a urine Na<10.
10. Use of amiloride and carbonic anhydrase inhibitors may be beneficial in diuretic resistant patients.
11. UF in CHF appears to be indicated primarily when dialytic therapy is also indicated for worsening cardiorenal syndrome.
12. Hypertonic saline with diuresis might be an interesting option -- robust trials still pending.
13. Skillful use of diuretics is the bottom line on how to succeed in treating CHF with renal dysfunction.

I had hoped the authors had commented on use of lung US in this disease. Diuretic use guided by Lung US findings might be more useful in many cases than later exam findings of edema( personal observation). 

Monday, November 6, 2017

TOPIC Discussion: LVAD and the Kidney



Left ventricular assist devices (LVADs) are common and implantation carries risk of AKI. LVADs are used as a bridge to heart transplantation or as destination therapy. Patients with refractory heart failure that develop chronic cardiorenal syndrome and CKD often improve after LVAD placement. Nevertheless, reversibility of CKD is hard to predict. After LVAD placement, significant GFR increases may be followed by a late return to near baseline GFR levels, and in some patients, a decline in GFR.
In a recent review in CJASN, we discuss changes in GFR after LVAD placement, the incidence of AKI and associated mortality after LVAD placement, the management of AKI requiring RRT, and lastly, we review salient features about cardiorenal syndrome learned from the LVAD experience.


Salient points   

Most of the AKI and CKD post LVAD is related to right ventricular failure. Identifying that and providing aggressive diuresis and or UF might be important.
Long term CKD related to LVAD might be related to hemolysis and R-CHF.
Hemodialysis and PD – both can be successfully be done in outpatient setting with LVADs
AVF should be still the first choice for LVAD patients in the outpatient settings that require dialysis e
The most important of all, interdisciplinary teams including cardiologist, surgeons, and nephrologists are critical in the success of an LVAD program.

Sunday, November 5, 2017

Nephrology on the rise, Positive trials, Positive job market!!

Nephrology really took an amazing turn this Kidney week in 2017. Positive trials, positive news and amazing things are happening for everyone involved in renal care.

First and foremost, the high impact clinical trials in 2017 ASN Kidney week revealed several positive trials.

The REPRISE study showed the impressive promise of use of tolvaptan in late stage ADPKD.  The liver related side effects were minimal. Hope to see this in clinical practice soon

The MENTOR trial that compared cyclosporine to rituximab for PLA2R membranous GN showed rituximab to be non inferior with lower rate of adverse effects. Looks like rituximab will be changing the treatment paradigm in membranous GN treatment.

Is contrast nephropathy dead? No not really. A randomized controlled trial showed that intra arterial contrast studies are more likely to cause contrast nephropathy compared to intra-venous, but both did have a incidence of contrast nephropathy.

A novel agent called QPI-1002 showed significant promise in decreasing AKI post CABG in high risk population.

Bardoxolone Methyl Improved GFR Measured by Standard Inulin Clearance: The TSUBAKI Study in Japan. The return of Bard!!

Another positive note: The GW-ASN fellows survey showed an upswing in job opportunities for our fellows in training. https://www.asn-online.org/education/training/workforce/

Finally, social media nephrology Guru Joel Topf wins Robert Narins award with an amazing video presentation done by ASN.


Wednesday, October 25, 2017

Consult Rounds: Podocytic infolding glomerulopathy( PIG)

Podocytic infolding glomerulopathy( PIG)

What is PIG? – This is a pathology based finding seen rarely in the EM section of the report. It is a form of  glomerulopathy, in which microspheres or microtubular structure or both are associated with infolding of cytoplasmic processes of podocytes into the glomerular basement membrane.  This type of glomerulopathy is not included in the World Health Organization’s classification of glomerular diseases but has been noticed in few cases reports and large case series from Japan.


Associations: In the largest series from Japan,  most patients might have a subtype of lupus, nephritis  class V, or membranous glomerulonephritis.  MCTD, Sjogren's syndrome and tumor lysis syndrome was also found. Interestingly, hydronephrosis was associated with most patients seen with this entity. There have been cases associated with Myeloma as well. 


Electron micrograph shows cytoplasmic  processes of podocytes infolded into the GBM. At the end of an infolded cytoplasmic process of podocyte, microspheres or microtubular structures or both were found. b The infolded cytoplasmic process of a podocyte went through the middle layer of the GBM, which was accompanied by thickening of the lamina densa.

The pathogenic mechanism of PIG is unknown. Hydronephrosis was found in three of 25 patients.  However, no study has shown that experimental hydronephrosis can induce podocytic infolding.In the large series from Japan, all had GBM thickening, and IF was negative in many, followed by some that had only C1q,c3 and some with a full house pattern.  Membranous GN is the most common light microscopy finding followed by FSGS and MPGN.  In an earlier report, some might have called this entity  Membranous glomerulopathy with spherules.

Some researchers performed an immunohistochemical study of complement C5b-9 complexes in several human kidney diseases and have shown positive reactions on round extracellular particles and on striated membranous structures in the GBM. Therefore, the mechanism of podocytic infolding might be related to the role of special types of complement activation in situ on the microstructure.  We don’t know if infolding of the podocyte cytoplasm may be a pattern of GBM/podocyte disruption rather than a true disease entity. However, the diffuse extent and severity of PIG raise the suspicion of defects in the repair mechanism.

Worth a read as we learn about this new entity!

Here are some interesting references



Sunday, October 1, 2017

In the NEWS: Point of Care ultrasound of the Lungs and the Nephrologists


Typical B-line (left) and the standard definition by Lichtenstein (right).Point of care US is increasingly being used in many medical specialties. Nephrology is catching along swiftly as well.  A recent review by our team led by Ross et al discuss the role of Lung US in the ESRD population.  After a systematic review,  we concluded that lung US can be used to determine volume status in chronic ESRD patients by using the B-line score model( see figure above from paper) as discussed in the paper.


As nephrologists, we should be using this in practice and help diagnose and prognosticate high risk patients and perhaps prevent re-admissions.

The role of lung ultrasonography in nephrology practice requires further research regarding its clinical applications. We stated in our paper the following amazing ways it can be used in clinical practice..
i.            What is the role of lung ultrasonography in the management of AKI in the intensive care unit? Could it be used as an endpoint for continuous renal replacement therapy?
ii.            Given the association of mortality with the presence of B-lines in the chronic dialysis population, what is the role of lung ultrasonography in the management of the patient on chronic HD? Could B-lines be used to guide need for increased ultrafiltration and would this change long-term outcome?
iii.            Could lung ultrasonography be used to guide diuretic therapy in patients with chronic cardiorenal syndrome?
iv.            As B-lines detect subclinical volume expansion, could lung ultrasonography be useful in differentiating hypervolemic from euvolemic hyponatremia?

Where can one learn to get point of care US training?
The Emory US course is the mecca of US training: check out the details here
NKF Spring Clinical Meetings 2017 had a course run by us as a pre-course specifically on point of care US. Similar course will be prepared for 2018
KidneyCon 2018 will also be having a hands on workshop for Point of care US training

Sunday, September 24, 2017

Consult Rounds: Cryoglobulins and the Kidney

Cryoglobulins and the Kidney

Cryoglobulins are Igs that reversibilly precipitate at temperatures <37C.  This results in symptoms that can lead to rashes, vasculitis, ulcers, ischemia, joint pains, and eventually in 25% cases – renal injury.




Two mechanisms: immune complex GN vs high viscosity related.  All have nephritic/nephrotic syndrome with various levels of kidney function.
1/3 with purpura and arthralgia
¾ with low C4 and ½ with low C3
All 3 types of cryoglobulins reported with renal disease
Most commonly it occurs in settings of type II (“mixed”) cryo secondary to hepatitis C virus.  Most patients with type II or III cryoglobulins have a positive rheumatoid factor.  The pathology pattern of injury is either membranoproliferative or diffuse proliferative GN.
          Type 1 Cryo( monoclonal IgM or IgG) – MM, MGUS, WM, lymphomas and CLL
          Type 2 Cryo(monoclonal IgM + polyclonal IgG)- CLL, lymphoma, SLE, Hep C

          Type 3 Cryo(polyclonal)- lymphoproliferative diseases, SLE

Treatment

Treatment of underlying cause- Hep, SLE, Myeloma
Steroids
Alkylating Agents
Anti CD-20 agents( good response in some cases)
Plasmapheresis ( adjunct) if skin involved and early renal
involvement

Sunday, September 10, 2017

Topic Discussion: Baclofen and ESRD

Baclofen is often used as a muscle relaxant in many patients. It has a half life of 3-7 hours and 80% excreted by the kidneys.  It is extremely important to dose adjust in CKD and avoid use in ESRD patients. Dialysis is a good mechanism to remove the agent as well in-case of ingestions and overdoses.

A recent case published in AJKD highlights this important drug related interaction in CKD and ESRD patients. 
The authors describe two excellent clinical algorithms.
The first algorithm discusses dose adjustments.
If GFR>90, no dose adjustment necessary
If GFR 60-90, decrease initial dose by 1/3
If GFR 30-60, decrease dose by ½ and watch for mental status changes
If on RRT or GFR<30, avoid use


The second algorithm discusses if there is a known baclofen toxicity( seizures, hypotenia, encephalopathy, etc.)

If severe AKI, CKD or ESRD- start daily HD or CRRT
If normal renal function or mild AKI but with respiratory depression or seizures- start daily HD or CRRT
If normal renal function or mild AKI and no severe symptoms- no dialysis

Tuesday, August 29, 2017

Consult Rounds: Tamoxifen induced hypercalcemia

A forgotten cause of hypercalcemia we need to remember is the drug- tamoxifen

This chemotherapy agent used in breast cancer has had a track record of causing hypercalcemia.
It was first described in 1980s.  In that large study, 470 patients with metastatic breast cancer treated with tamoxifen, ten patients (2.3%) developed hypercalcemia. All patients with hypercalcemia had osteolytic or mixed lytic and blastic bone metastases. Hypercalcemia developed after a median period of seven days (range 4-11 days) of tamoxifen administration. Hypercalcemia was treated with conventional measures and serum calcium levels normalized in nine patients, either with a brief interruption of tamoxifen therapy or in spite of continued treatment. Four patients experienced partial remissions with continued tamoxifen therapy. These results indicate that hypercalcemia is a potentially serious complication of tamoxifen therapy but is generally short-lived, and can be controlled with supportive measures, thus allowing continued tamoxifen administration.

Other published reports are

One recent study looked at a large series of breast cancer patients who were hypercalcemic post tamoxifen- happened within 9 days of start and peaked at a level of 13. All patients also had bone lesions as well.  Gallium nitrate was used to reverse the abnormality while keeping tamoxifen on.


No mention of this in any renal literature. Unclear mechanism of this entity. 

Monday, August 28, 2017

Topic discussion: Downsizing in Nephrology

A timely editorial just got published in CJASN. 
Three large NYC related programs give their thoughts on downsizing in nephrology fellowship spots. A comparison is made with anesthesiology that helped revert their trend of decrease supply in the 1990s.  The authors bring up few major concerns

1.       The debt burden of recent graduates and the compensation that nephrologists receive is not attractive. But the authors make a good point that while the starting salaries are low, there is room for growth and potential that other fields might not have. This is speculative and might depend on coast to coast in the US. While certain parts of the country, nephrologist make a lucrative salary, there are others where hospitalists make much more than nephrologists.

2.       The authors make an interesting suggestion of broadening our certification. This is an excellent thought. I urge the nephrology community to try to do this in the 2-3 year time frame of a fellowship. There are a minority of candidates who would do an extra year given their debt burden but incorporating something extra in your fellowship might help that candidate get that certificate along with Nephrology- be it glomerular disease, onconephrology or critical care.

3.       Chronic disease models have done well with PA and NP based teams in certain parts of the country. Examples are oncology, BMT, renal transplant, CT surgery. Nephrology should learn from these models. As the authors suggest, perhaps cautious downsizing might help reverse trend of supply/demand and help get outstanding candidates back in Nephrology.  A formula was suggested back few years ago by Desai and perhaps can be considered if need be.

4.       Overnight call is part of being a nephrologist. While authors suggest that the fellows might be called in a lot- one cannot ignore a K of 8 and wait till the 8AM fellow/attending comes in. Remote management might be possible but we have to be cautious in those methods.  Transplant overnight call should be reduced and can be the most helpful. A DDRT call should really not involve the nephrology fellow unless dialysis is required pre transplant. 

5.       Regardless of number of applicants a program is getting- the dependence on fellows for day to day work should be abolished.  This makes the applicant feel that the program is “fellow” centric and not “fellow” dependent. Attending directed services, NP, and PA based practice can help foster this environment. The flip side is loss of intensive education.  Given the rounding in the dialysis unit to only an NP or PA and relieving the fellow might lead to long term loss of education that we may regret. If planning this, would careful involve fellow in some of the rounding as well.  In addition, taking care of certain volume of patients and putting a cap on consults can also lead to “inefficient” graduates and unable to handle the volume when in private practice.  Fellows also have to learn how to manage and prioritize sick vs not that sick patients and how to manage a long and busy list. Nephrologists are smart physicians. We also want our fellows to be effective communicators, and efficient doctors.



I commend the authors on this very provocative essay and hoping this dialogue continues in making nephrology more attractive as it was many years ago.  

Wednesday, August 9, 2017

Monday, August 7, 2017

Saturday, August 5, 2017

Friday, August 4, 2017

Consult Rounds: Parvovirus b19 and Glomerular disease


Image result for parvovirus b19Parvovirus b19 has been associated with the following glomerular findings


1.  Collapsing GN
2. Proliferative GN
3. FSGS
4. Thrombotic Microangiopathy

https://www.ncbi.nlm.nih.gov/pubmed/17699510 in an amazing review article that summarizes all renal associated findings with parvovirus b19 especially in the transplanted kidney.

Friday, July 14, 2017

Topic Discussion: CAR-T therapy and the Kidney



A new dawn is breaking in the field of hematologic malignancies, as the first product based on chimeric antigen receptor (CAR) T cells was scrutinized today by a panel of experts and unanimously recommended for approval at the FDA for pediatric and young adult patients (age 3-25 years) with relapsed or refractory acute lymphoblastic leukemia (ALL).


Blood is collected from the patient, and then autologous T cells are separated out and genetically engineered. The process involves inserting a CAR that targets CD19, an antigen expressed on B cells and tumors derived from B cells.  These CAR T cells are then infused back into the patient, who has undergone chemotherapy, and in the body the product homes in on B-cell leukemic cells and destroys them.  The main action happens mostly about 2 weeks after those CAR-T cells have been re-infused.  Some have termed this form of therapy as the “ living drug”

Autologous CAR-T cell therapy first shot into headlines about 4-5 years ago when it was thought about in CLL patients.   Then several other studies were done essentially confirming that the concept is correct but there are serious toxicities.


The technology is complicated and initially when tried in CLL led to multiple toxicities of various organs including CNS, cardiac, renal and mostly requiring ICU admissions from acute cytokine release syndrome. This happens due to high levels of IL-6, a cytokine that is secreted by T cells and macrophages in response to inflammation.  Etanercept and tocilizumab have been used to block the IL-6 activity to treat such side effects.

Acute renal injury following CAR T-cell infusion is multifactorial and almost always reversible. Reduced renal perfusion is often the most important cause of renal injury. Reduced renal perfusion can be caused by cytokine-mediated vasodilation, decreased cardiac output, or intravascular dehydration due to insensible losses from high fevers. Tumor lysis syndrome and drug effect from medications such as antibiotics are other possible causes of renal injury. Electrolyte disturbances, such as hyponatremia, hypokalemia, and hypophosphatemia are not uncommon but have been reported. A recent article in Blood summarizes all toxicities.

Now the therapy has returned and we may see this in many centers. We must be aware of the cytokine release storm that it can cause leading to AKI in that setting.  There might be more in the pipeline of similar products such as the one that just got approved for ALL.




Consult Rounds: Cholemic nephrosis or Bile cast nephrpathy or should we say Jaundice associated nephropathy













Bile cast nephropathy or also called cholemic nephrosis represents a spectrum of renal injury from proximal tubulopathy to intrarenal bile cast formation found in patients with severe liver dysfunction. Bile can be toxic directly to the tubule or can form casts and have similar damage as myeloma cast nephropathy.


1.      Classically seen with patients with acute or chronic liver disease
2.      Usually, the total bilirubins are over 20 and conjugated over 16 is the cases that had bilirubin casts on kidney biopsies
3.      The LFTS were also higher in these patients
4.      The cause of liver disease doesn’t matter

The mechanisms responsible for tubular dysfunction include uncoupling of mitochondrial phosphorylation (thereby decreasing ATPase activity) by bilirubin  and oxidative damage of tubular cell membranes as well as inhibition of Na-H and Na-K pumps in the tubular cell membranes by bile acids. Cholemic nephrosis is reversible provided bilirubin levels are reduced early. This recovery is however delayed if there is extensive bile cast formation.
Some have suggested jaundice-related nephropathy as a replacement for cholemic nephrosis. Based on their definition, jaundice-related nephropathy would encompass the spectrum of injury that ranges from proximal tubulopathy to extensive tubular injury and tubular pigment. 
As bile passes via tubules, there is pigment nephropathy.

Pathology findings include: extensive acute tubular injury with bile stained tubular casts.
Macroscopic findings will include bile stained yellowish discoloration of the kidneys in jaundiced patients which become dark green after formalin fixation.
The Hall's stain confirms bilirubin presence.

Other interesting articles on this topic

Saturday, July 1, 2017

Consult Rounds: Acyclovir and dialysis



An often unforgotten drug that we must be aware of in ESRD patients is acyclovir.
Acyclovir can accumulate in ESRD if not dosed appropriately and can lead to neurotoxicities- leading to confusion, tremors and coma.

Initial study of 7 patients with end stage kidney disease receiving hemodialysis looked at levels following hemodialysis with each patient received a single 800-mg tablet of acyclovir. Plasma acyclovir levels were monitored over the next 48 h as well as before and after the next routine dialysis. Peak plasma levels were achieved at 3 h (12.54 +/- 1.76 microM, range 8.5-17.5 microM) with the half-life calculated to be 20.2 +/- 4.6 h. Mean plasma level of 6.29 +/- 0.94 microM were within the quoted range to inhibit herpes zoster virus (4-8 microM) at 18 h. Hemodialysis (4-5 h) eliminated 51 +/- 11.5% of the acyclovir which remained at 48 h. Computer modelling of various dose modifications suggests that a loading dose of 400 mg and a maintenance dose of 200 mg twice daily is sufficient to maintain a mean plasma acyclovir level of 6.4 +/- 0.8 microM. A further loading dose (400 mg) after dialysis would raise the residual acyclovir concentration by 6.1 +/- 1.0 microM.

Acute acyclovir neurotoxicity can be treated in CKD and ESRD patients with dialysis. The drug is water soluble, not albumin bound and small- hence an ideal dialysis candidate for removal.  It is important to keep this toxicity in mind as many might come in to your office with non renal dosing of this agent on ESRD and CKD patients and can lead to neurotoxicity. PD is not an option; HD is preferred mode for removal of acyclovir. 

  Some references

Tuesday, June 27, 2017

Topic Discussion: New Glomerular diseases cases with targeted therapies

Targeted therapies can lead to a glomerular disease. Previously, two reviews didn’t find any glomerular diseases associated with BRAF inhibitors and PD-1 inhibitors.  In the last 6 months, 3 recent papers have highlighted interesting cases of both BRAF-MEK combination and PD-1 inhibitors leading to glomerular diseases.

  

While the PD-1 inhibitor case is the first of it’s kind, we must be mindful of GN in these patients as well. In terms of the BRAF+MEK combo, both authors of the above listed papers. Showed that it was the BRAF inhibition that decreased PLCε1 expression in podocytes, accompanied by a reduction in nephrin expression and an increase in permeability to albumin. Additionally, these drugs inhibited the podocyte–vascular endothelial growth factor (VEGF) system leading to perhaps a component of TMA as well.


Tuesday, May 30, 2017

ASN Robert G Narins Award for 2017 goes to Blogger, educator Joel Topf

The Robert G. Narins Award by ASN honors individuals who have made substantial and meritorious contributions in education and teaching. This award is named for Robert G. Narins, who is also the first recipient of the award.

Dr. Narins' contributions to education and teaching started in 1967 from chairing for eight years the ABIM's Nephrology Board and working on the ACP's Annual Program Committee. His contributions to education in the fields of fluid-electrolyte and acid-base physiology are prodigious and well-recognized.  Dr. Narins was also involved in the creation and planning of many ASN educational programs during Renal Week and throughout the year, including: Board Review Course and Update, one and two day programs at Renal Week, Renal WeekEnds, and NephSAP.

Prior Award winners of this award are( from ASN website)

·    2015 Mark L. Zeidel, MD, FASN
·    2014 Stuart L. Linas, MD, FASN
·    2013 Mark E. Rosenberg, MD, FASN
·    2012 Donald E. Kohan, MD, PhD, FASN
·    2011 Agnes B. Fogo, MD
·    2010 Barry M. Brenner, MD
·    2009 Burton D. Rose, MD
·    2008 Mitchell L. Halperin, MD
·    2007 Richard J. Glassock, MD
·    2006 Robert G. Narins, MD

This year marks a landmark in this award as it’s being presented to Joel Topf, MD.

Image result for joel topf

While all other educators followed a conventional track for teaching and educating, Joel’s contribution to nephrology education has been very unique and different.  Here is what Joel has accomplished in the last 10 years!
1.       Creation and maintaining the Precious Body Fluids Blog with educational material that spans from electrolyte disorders to AKI
2.       The best acid base book written in Nephrology as a “resident”. This is by far the easiest book to understand acid base disorders.
3.       Co creation of the first ever academic journal blog- AJKD blog
4.       Creation of Nephmadness since 2013 ( first ever online game in Nephrology) with educational material that spans all parts of renal medicine
5.       Creation of NephJC( the first and most successful online journal club that meets every 2 weeks)
6.       Co creation of DreamRCT( how to propose and create a dream RCT that we need in nephrology competiton)
7.       Creation of Nephrology Social Media Collective Internship to train trainees, and faculty on become social media experts to improve medical education
8.       Teaching and promoting social media education in nephrology
9.       Showcasing how twitter can be used in nephrology education at it’s best! (https://twitter.com/kidney_boy)
10.   Several teaching awards at his local institution

Most important of all: He has inspired and trained many young and old teachers/and educators due to his passion for nephrology!
Way to go Joel and congrats!

Wednesday, May 17, 2017

Consult Rounds: Topiramate and the Kidney

Topiramate was first introduced to treat seizures but now is increasingly used to treat migraines and is among the top 6 drugs sold in the United States. In addition, it is used as a weight loss agent as well. Renal toxicity with this agent is not uncommon.

The three forms of renal toxicity are:

Kidney Stones
Renal Tubular Acidosis
Isolated hypokalemia

A study in 2006 published in AJKD showed that topiramate acts through multiple mechanisms, 1 of which is the inhibition of carbonic anhydrase, as in vitro studies have shown. Several case reports described a link between topiramate and the formation of calcium phosphate stones, but the mechanism for this is largely unknown.

The authors conclude that taking topiramate for about 1 year caused systemic metabolic acidosis, significantly increased urine pH, and markedly lowered urine citrate — changes that increase the propensity to form calcium phosphate stones.

With the increasing use of topiramate, reports have emerged that topiramate can cause metabolic acidosis in some patients. It does this by impairing both the normal reabsorption of filtered HCO(3)(-) by the proximal renal tubule and the excretion of H(+) by the distal renal tubule. This combination of defects is termed mixed proximal and distal RTA. Topiramate-induced RTA can make patients prone to kidney stones as stated earlier as well.  The utility of regular monitoring of HCO(3)(-) levels has not been proven and is not routine practice currently.

Finally, isolated refractory renal wasting of potassium has also been reported with this agent.

A large systematic review confirmed the above findings of renal toxicity with this agent. Fourty-seven reports published between 1996 and 2013 were retained for the final analysis. Five case-control studies and six longitudinal studies addressed the effect of topiramate on acid-base and potassium balance. A significant tendency towards mild-to-moderate hyperchloraemic metabolic acidosis (with bicarbonate ≤21.0 mmol l(-1) in approximately every third case) and mild hypokalaemia (with potassium ≤3.5 mmol l(-1) in 10% of the cases) was noted on treatment with topiramate, which was similar in children and adults.

Finally,increasing evidence supports the use of topiramate. Topiramate is generally well tolerated, and serious adverse events are rare. Nonetheless, it is linked with the development of acidosis, hypokalaemia, hyperuricaemia and hypocitraturia and eventually renal stones.



Monday, May 15, 2017

Master teacher: how do you define one?

Image result for master teacher

What makes a “master clinician teacher”—adapted from George Couros, an educator.

This list can be used for teachers in med students, residency and in nephrology fellowship as well.

·         Connects with students and gets to know them individually.
·         Helps students to meet their own individual needs as each might have their own learning styles
·         Makes the curriculum and what is taught relevant.
·         Works with students to develop their love of learning, helping students to find their own spark in learning( concept of intrinsic motivation –often lacking in our trainees)
·         Keeps themselves as a teacher up-to-date. Education and learning will always change ( being a learner for life makes you a better teacher)
·         Focuses on learning goals as opposed to performance goals.
·         Ensures that “character education” is an essential part of learning. Students need to grow emotionally as well as mentally( this is critical in creating the culture for constant life long learning and work life balance)
·         Is passionate about the content they teach( THIS is by far the MOST important quality)
·         Is concerned not just with what is taught in their class but with their overall impact on the school culture( Making a cultural difference is critical on perhaps methods of teaching)
·         Communicates well with all the stakeholders and not just the students( a subtle but needed politician)

·         Behaves as a facilitator of learning- not a “spoon feeder”


All our fellows out there, I am sure you have one mentor who exemplifies these qualities. This is what makes the experience of learning a more meaningful experience. Please take a minute to salute and respect all our teachers and educators in our lives. They teach you medicine but they also may be teaching you a way of life!

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